Operation for polysyndactyly of the fifth toe using Z-plasty.

A new operative procedure was devised to treat polysyndactyly of the fifth toe. This procedure, which consists of removal of the fifth toe, correction of the alignment of the preserved sixth toe by arthroplasty and construction of an interdigital space by Z-plasty, is technically simple and produces good results, both functionally and aesthetically.     

Reperfused myocardial infarctions on T1- and susceptibility-enhanced MRI: Evidence for loss of compartmentalization of contrast media

The purpose of this study was to characterize the contrast caused by a susceptibility MRI contrast agents, on spin echo T₂-weighted imaging of reperfused myocardial infarction. Our interest in this model focused on the expected requirement that such agents be compartmentalized in the tissue to cause signal loss on spin echo images, a condition which may not be present in reperfused infarcted myocardium. Accordingly, nine rats were subjected to 2 h of left coronary artery occlusion followed by 3 ± 0.5 h of reperfusion prior to administration of contrast media. Three sets of MR images were acquired: (a) baseline axial images at the midventricle, both T₁-weighted (TR/TE = 300/20) and T₂-weighted (TR/TE = 1500/60); (b) T₁-weighted images after administering a T₁-enhancing agent, Gd-DTPA-BMA (0.2 mmol/kg), to document that contrast media is delivered to the reperfused infarction; and (c) T₂-weighted images after administering the susceptibility agent, Dy-DTPA-BMA (1.0 mmol/kg). Gadolinium-enhanced T₁ images depicted reperfused infarction as regions with greatly enhanced signal intensity compared with unin-farcted myocardium, indicating that contrast agent was delivered to the infarcted zone. Dysprosium-enhanced T₁ images depicted the injury as a region of persistent signal intensity relative to depletion of signal in normal myocardium, consistent with failure of the contrast agent to cause signal loss. Similar infarction sizes were observed for unenhanced T₂-weighted images (33 ± 5%), gadolinium-enhanced T₁ weighted images (36 ± 5%) and postmortem staining (30 ± 6%); strong correlations (r > 0.9) were noted in comparisons of these data. Dysprosium-enhanced images exhibited a smaller region of differential signal presumed to be infarction (20 ± 5%, P < 0.05) and weak correlations (r < 0.75) with the other measurements. We conclude that the smaller infarction depicted on dysprosium-enhanced images is a subregion of the true infarction in which myocardial necrosis is sufficiently advanced that the agent is homogeneously distributed throughout all tissue compartments, preventing T₂*-dependent phase loss on spin echo images.     

Case of ruptured gastroduodenal arterial pseudoaneurysm with penetration to the duodenum, successfully treated with transcatheter arterial embolization]

A 77-year-old man, who underwent segmental pancreatectomy for intraductal papillary mucinous adenoma in 2001, was referred to our hospital with complaints of hematemesis and melena on January, 2004. Emergency upper gastrointestinal endoscopy showed a pulsating submucosal protrusion in the duodenal bulb, which was identified as a gastroduodenal arterial aneurysm measuring 1.5cm on abdominal CT imaging. Transcatheter arterial embolization of the aneurysm with metallic coils was successfully performed. Periodically repeated endoscopic examination has revealed the coils protruding into the duodenal lumen without any serious complication.     

A CASE OF METASTATIC YOLK SAC TUMOR OF TESTIS IN A CHILD

We report a case of testicular yolk sac tumor in a child aged 3 years and 6 months with multiple bulky metastases to lung and retroperitoneum (stage 11182). After three courses of chemotherapy with a PV 8 regimen (cisplatin, vinblastine and bleomycin). complete and partial responses were obtained for lung and retroperitoneal lymph node metastases, respectively. The patient was followed-up closely. However, on the basis of a re-elevated alpha-letoprotein (AFP) after 4 months' follow-up, he was treated with three courses of salvage chemotherapy with a modified VAB-6 regimen (cyclophosphamide. etoposide. actinomycin D, bleomycin and cisplatin), lollowed by retroperitoneal lymph node dissection. Histologically, only necrotic tissue was found. There is no evidence of recurrence 24 months after lymphadenectomy. There is very little information in the literature on the appropriate management of postchemotherapy residual mass in pediatric testicular tumors.     

Validity of Electrode Placement at Fpz to Detect Alpha Wave

Abstract: The possibility on placing electrodes at Fpz-A₂ instead of C₃-A₂ was investigated to obtain a more stable configuration avoiding obstruction by the hair. Our original system of alpha wave detection by a microcomputer was used, and a total of 22 all-night hypnograms of five healthy young students waa recorded. Pearson's moment correlation coefficients of alpha wave % between the two positions were 0.780–0.948. Except for one subject, alpha wave % taken at Fpz-A₂ tended to be 3–5% lower than that at C₃-A₂. The above analysis indicates that using EEG electrode position of Fpz-A₂ is valid and useful as a stable electrode configuration for a long-time monitoring.     

Experimental study of spinal cord compression by epidural tumors using electron probe X-ray microanalysis and confocal laser scanning microscopy

Changes in the nerve fibers of the spinal cord were studied in rat experimental epidural tumor models. Light microscopy showed demyelinization in all with rats paraparesis and paraplegia. Cross-sectional views of nerve fibers stained with 3,3dipentyloxacarbo-cyanine iodide, obtained by confocal laser scanning microscopy, showed distorted, shrunken fibers with a low fluorescence intensity. Changes in the electrolyte contents of nerve fibers were studied by electron probe X-ray microanalysis. The K concentration in axons and the myelin sheath was increased in the paraparesis group, but was decreased in the paraplegia group. These findings suggest that, in the paraparesis group, compression of the spinal cord damaged cell membrane channels, which subsequently caused an increase in intracellular K, a decline in the action potential, and low-intensity fluorescence of nerve fibers. On the other hand, in the paraplegia group, destruction of cell membranes caused a decrease in intracellular K until it approached the extracellular level. This reduced both the action potential and the fluorescence intensity. As Ca and Mg concentrations in both axons and the myelin sheath increased in relation to the severity of neurologic damage, it appears that these electrolytes may also play an important role in damage to nerve fibers.     

Glutamate immunoreactive terminals in the lateral amygdaloid nucleus: a possible substrate for emotional memory.

The ultrastructure and synaptic associations of terminals immunoreactive for L-glutamate (Glu) were examined in the lateral nucleus of the amygdala (AL). All results reported here involved tissue fixed only with paraformaldehyde. The specificity of the antiserum with paraformaldehyde fixation conditions was assessed and confirmed by immuno-dot blot analysis: the reactivity of anti-Glu to glutamic acid was at least 1,000 times greater than the reactivity to other amino acids. At the light microscopic level, Glu-immunoreactive punctate processes and somata were present in AL. At the electron microscopic level, many Glu-immunoreactive terminals were identified. Data analysis was performed on 365 of these labeled terminals. Glu-immunoreactive terminals were 0.3-1.5 microns in diameter and contained numerous small, clear vesicles as well as mitochondria. Many (77%) of the terminals analyzed had morphologically identifiable synaptic specializations. Most (90%) of the Glu-immunoreactive terminals with synaptic specializations formed asymmetric synapses on spines or small dendrites; synaptic specializations on soma or proximal dendrites were rarely seen (< 1%). Glu-immunoreactive terminals were qualitatively compared to terminals in AL labeled with two other antisera: anti-glutaminase, a marker for the enzyme that catalyzes the conversion of glutamine to the releasable or transmitter form of Glu, and anti-gamma-aminobutyric acid (anti-GABA), a marker for the major inhibitory amino acid transmitter in the brain. Terminals immunoreactive for glutaminase, like those immunoreactive for Glu, formed mostly asymmetric synaptic specializations on spines or small dendrites. In contrast, GABA-immunoreactive terminals usually formed symmetric synapses on soma or proximal dendrites and were never observed to form asymmetric axo-spinous contacts. Although Glu is a metabolic precursor to GABA, these data indicate that the majority of Glu-immunoreactive terminals reflect the site of synthesis and release of Glu and not of GABA. In addition, these results provide morphological evidence that Glu plays a role in excitatory neurotransmission at synapses in AL and support the growing body of data implicating excitatory amino acid-mediated synaptic plasticity in-emotional learning and memory processes in AL.